java barcode scanner library C Intrinsic Renal Failure in Objective-C

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C Intrinsic Renal Failure
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Intrinsic renal disorders account for up to 50% of all cases of acute renal failure Intrinsic (or parenchymal) dysfunction is considered after prerenal and postrenal causes have been excluded The sites of injury are the tubules, interstitium, vasculature, and glomeruli
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ACUTE TUBULAR NECROSIS
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when using these agents The mainstay of therapy is a liter of 09% saline over 12 hours both before and after the contrast administration cautiously in patients with preexisting cardiac dysfunction Neither mannitol nor furosemide offers benefit over saline hydration In fact, furosemide may lead to increased rates of renal dysfunction in this setting In some but not all studies, N-acetylcysteine given before and after contrast decreased the incidence of dye-induced nephrotoxicity Its benefit seems more pronounced in subjects with a lower GFR Acetylcysteine is a thiol-containing antioxidant with little toxicity whose mechanism of action is unclear With little harm and possible benefit, administering acetylcysteine 600 mg orally every 12 hours twice, before and after a dye load, for patients at risk for acute renal failure, is a reasonable strategy Intravenous N-acetylcysteine has shown benefit compared with placebo, and may be a good option if a patient acutely needs contrast dye Investigators have shown a benefit using sodium bicarbonate rather than normal saline as the isotonic volume expander Other nephrotoxic agents should be avoided during the day before and after dye administration Cyclosporine toxicity is usually dose dependent It causes distal tubular dysfunction from severe vasoconstriction Regular blood level monitoring is important to prevent nephrotoxicity With patients who are taking cyclosporine for renal transplant rejection, kidney biopsy is often necessary to distinguish transplant rejection from cyclosporine toxicity Renal function usually improves after reducing the dose or stopping the drug Other exogenous nephrotoxins include antineoplastics, such as cisplatin and organic solvents, and heavy metals such as mercury, cadmium, and arsenic
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Clinical scenario consistent with diagnosis (ischemic or toxic insult) Urine sediment with pigmented granular casts and renal tubular epithelial cells is pathognomonic but not essential
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Acute renal failure due to tubular damage is termed acute tubular necrosis and accounts for 85% of intrinsic acute renal failure The two major causes of acute tubular necrosis are ischemia and toxin exposure Ischemia causes tubular damage from states of low perfusion and is often preceded by a state of prerenal azotemia Ischemic acute renal failure is characterized not only by inadequate GFR but also by renal blood flow inadequate to maintain parenchymal cellular formation This occurs in the setting of prolonged hypotension or hypoxemia, such as dehydration, shock, and sepsis Major surgical procedures can involve prolonged periods of hypoperfusion, which are exacerbated by vasodilating anesthetic agents The other major cause of acute tubular necrosis is nephrotoxin exposure Exogenous nephrotoxins more commonly cause damage than endogenous nephrotoxins
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A Exogenous Nephrotoxins
Up to 25% of hospitalized patients receiving therapeutic levels of aminoglycosides sustain some degree of acute tubular necrosis Nonoliguric renal failure typically occurs after 5 10 days of exposure Predisposing factors include underlying renal damage, dehydration, and advanced age Aminoglycosides can remain in renal tissues for up to a month, so renal function may not recover for some time after stopping the medication Monitoring of peak and trough levels is important, but trough levels are more helpful in predicting renal toxicity Gentamicin is as nephrotoxic as tobramycin; streptomycin is the least nephrotoxic of the aminoglycosides, likely due to the number of cationic amino side chains present on each molecule Amphotericin B is typically nephrotoxic after a dose of 2 3 g This causes severe vasoconstriction with distal tubular damage and can lead to distal renal tubular acidosis with hypokalemia and nephrogenic diabetes insipidus Vancomycin, intravenous acyclovir, and several cephalosporins have been known to cause acute tubular necrosis Radiographic contrast media can be directly nephrotoxic Contrast nephropathy is the third leading cause of new acute renal failure in hospitalized patients It probably results from the synergistic combination of direct renal tubular epithelial cell toxicity and renal medullary ischemia Predisposing factors include advanced age, preexisting renal disease (serum creatinine > 2 mg/dL), volume depletion, diabetic nephropathy, congestive heart failure, multiple myeloma, repeated doses of contrast, and recent exposure to other nephrotoxic agents, including NSAIDs and ACE inhibitors The combination of diabetes mellitus and renal dysfunction poses the greatest risk (15 50%) for contrast nephropathy Lower volumes of contrast with lower osmolality are recommended in high-risk patients Toxicity usually occurs 24 48 hours after the radiocontrast study Nonionic contrast media may be less toxic, but this has never been proved Prevention should be the goal
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